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Cardiology Flashcards

1
Q

on an ecg one large square is how much in time

A

0.2seconds or 200ms

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2
Q

on an ecg one small square is how long in time

A

0.04 seconds or 40ms

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3
Q

how many large squares per second in an ecg

A

5 large squares per second

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4
Q

what is the PR interval and how long should it be

A

time from the onset of the P wave to the start of the QRS complex

it should normally be 120-200ms

this is 3-5 small squares

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5
Q

draw the ecg axis diagram

A
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6
Q

normal axis is from what degrees to what degrees

A

-30 degrees to +90 degrees

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7
Q

left axis deviation will look like what

A

QRS predominantly negative in VF II and III
QRS predominantly positive in VL and I

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8
Q

right axis deviation will look like what

A

QRS predominantly negative in I
QRS predominantly positive in III

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9
Q

which leads look at the septum

A

V3 and V4

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10
Q

what is the transition point

A
  • the v1 lead looks at the heart from the right
    • it begins with a small septal r wave as the septum is depolarised left to right initially
    • then as the left ventricle depolarises there follows a large downwards S
    • the v1 complex is therefore predominantly negative
  • the v6 lead looks at the heart from the left
    • it begins with a small downwards Q as the septum is initially depolarised left to right
    • then there is a large upwards R wave as the left ventricle is depolarised
    • the v6 complex is therefore predominantly positive
  • the transition point is the point at which the R waves and the S waves are of equal size
  • it is usually around v3-v4
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11
Q

what is the significance of the transition point

A
  • it can shift with changing shape of the heart
  • with right ventricular hypertrophy the transition point would shift to the left
  • this would mean that it would be around v5-v6 rather than v3-v4
  • it is as if, seen from the perspective of the feet, the heart has rotated clockwise
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12
Q

what is first degree heart block

A

it is when the pr interval is longer than 200ms

it’s ‘marked first degree heart block’ if >300ms

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13
Q

what is second degree heart block

A
  • mobitz i (wenckeback)
    • progressive lengthening of pr
    • followed by a dropped QRS complex
    • pr then goes back to being shorter and the cycle continues
  • mobitz ii
    • PR interval is constant but there is an occasional dropped QRS
      • there may be two or three or four P waves for every successful QRS in which case it is given a ratio 2:2 or 3:1 etc
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14
Q

what is third degree heart block

A

atrial contraction may be normal but no beats are conducted to the ventricles themselves

ventricular contraction is maintained by ventricular escape rhythms

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15
Q

what does blockage of both bundle branches look like

A

it has the same effect as a complete block of the his bundle and resembles complete heart block

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16
Q

why does right bundle branch block look like that

A
  • best seen in v1 where there is an RSR pattern
    • upwards deflection as septum initially depolarised from left to right
    • then s wave as the left ventricle is depolarised as normal
    • it takes longer for the right ventricle to be depolarised so there then follows a second R wave as the right ventricle is depolarised after the left
  • in v6 there is a wide deep qrs
    • initially a q as the septum is depolarised left to right
    • then an R wave as the left ventricle is depolarised
    • then follows a deep wide s wave as the right ventricle catches up
  • right bundle branch block is only significant if the qrs is longer than 120ms
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17
Q

why does left bundle branch block look like that

A
  • if conduction down the left bundle branch fails then the septum is depolarised from right to left
    • in V1 this appears as a small q wave
      • then the right ventricle is depolarised before the left so there is then an r wave in v1
      • subsequent depolarisation of the left ventricle then causes an s wave in v1
    • in V6 the initial right to left depolarisation of the septum causes a small r wave
      • then follows a small (like a notch) s wave as the right ventricle is depolarised
      • then v6 shows another R wave as the left ventricle catches up
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18
Q

in summary how does right bundle branch block appear

A

best seen in v1

there is an RSR pattern

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19
Q

in summary how does LBBB appear

A

best seen in v6 where there is a broad qrs with a notched top

the complete picture with a w shape in v1 is often not fully visible

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20
Q

what happens in atrial tachycardia

A

depolarisation is from an origin in the atria that is different to the sa node

the av node cannot conduct rates fasterr than 200/min so there may be a physiological block

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21
Q

what happens in atrial flutter

A

if there atrial rate is >250/minute then there is no baseline between p waves

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22
Q

what happens in junctional/nodal tachycardia

A

the depolarisation originates from the area around the av node

therefore the atria and the ventricles are depolarised at the same time

therefore p wave will be very close to the QRS complex or may be lost within it

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23
Q

what happens in wolff parkinson white syndrome

A
  • some people have an accessory bundle connecting the atria and the ventricles
  • there is no AV node delaying contraction
  • this provides pre-excitation to the ventricles
  • therefore there is a short PR interval and the QRS has a wide slurred upstroke called a delta wave
  • the second part of the QRS is normal as the excitation from the his bundle catches up
  • the his bundle and the accessory bundle can together form a re-entry circuit that causes tachycardias
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24
Q

what are the 6 questions to ask yourself when identifying abnormal ecg rhythms

A
  1. is the abnormality occasional or sustained
  2. are there p waves
  3. what is the P:QRS ratio
  4. are the ventricles contracting regularly or irregularly
  5. is the QRS a normal shape
  6. what is the ventricular rate
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25
Q

identify the rhythms

A
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26
Q

what are the two important abnormalities in form of the p wave

A
  • peaked p wave
    • right atrial hypertrophy
    • pulmonary hypertension
    • tricuspid valve stenosis
  • broad and bifid p wave
    • left atrial hypertrophy
      • usually due to mitral stenosis
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27
Q

what are the 4 characteristics of a normal QRS

A
  1. duration no longer than 120ms (3 little squares)
  2. in a right ventricular lead the (V1) the S is greater than the R
  3. in a left ventricular lead (V6) the R is less than 25mm
  4. left ventricular leads show a Q wave due to septal depolarisation which is initially left to right but these are less than 1mm across and 2mm deep
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28
Q

what are the ECG findings of PE

A
  • in many cases there is a normal ecg
  • sinus tachycardia is the most common finding
  • but there may be findings of acute cor pulmonale
    • S1Q3T3
      • large S wave in lead 1
      • pathological Q wave in lead 3
      • inverted T wave in lead 3
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29
Q

what are the ecg findings of right ventricular hypertrophy

A
  • peaked p waves (as it normally accompanies right atrial hypertrophy)
  • right axis deviation
  • tall r waves in v1
  • maybe right bundle branch block
  • inverted T waves which are normal in v1 spread across to v2 and v3
  • transition point shifts to the left with a deep s wave persisting in v6
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30
Q

in which leads are q waves normal

A

in the left ventricular leads

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31
Q

when are q waves abnormal

A

when they are greater than 1 small square in width (40ms) and 2mm in depth

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32
Q

what does a q wave of more than 1 small square in width (40ms) and 2mm in depth signify

A

MI

can be old or new as once q waves appear they rarely go

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33
Q

why are q waves from MI

A
  • because ventricles depolarise from inside to outside
  • therefore an area that’s not depolarising will record as a cavity potential
  • therefore a lead looking at that area will record a q wave
  • this will therefore be the case for anterior, lateral and anterolateral MIs
  • not posterior MIs as there’s no leads looking at the back typically
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34
Q

how does a posterior MI look on ECG

A
  • there may or may not be ST elevation
  • left ventricular depolarisation no longer overshadows right ventricular in V1
  • therefore V1 shows a tall R wave
  • this is similar to as in right ventricular hypertrophy but doesn’t have the other features of rvh
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35
Q

st elevation is due to

A

MI or pericarditis

pericarditis it will be in all of the leads whereas in MI it’s usually localised

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36
Q

horizontal depression of the ST segment means

A

ischaemia rather than infarction

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37
Q

downward sloping ST segments are due to treatment with digoxin

A
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38
Q

T waves are normally inverted in which leads

A
  • VR
  • V1
  • sometimes in III
  • sometimes in V2
  • in V3 in some black people
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39
Q

what is the effect of digoxin in the ecg

A

af

downward sloping st

inverted t waves

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40
Q

what’s the process of stemi ecg changes

A
  • the first abnormality seen in st elevation
  • then Q waves appear and the T wave becomes inverted
  • the st segment then returns to baseline
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41
Q

nstemi ecg changes

A

not full thickness so no Q wave and no ST elevation

but there will still be t wave inversion

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42
Q

main ecg finding of left ventricular hypertrophy

A
  • there may be left axis deviation
  • but the main thing is that there will be inverted t waves in the lateral leads
    • I, II, aVL, v5 and v6
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43
Q

why can t wave inversion be seen in bundle branch block

A

because abnormal depolarisation can lead to abnormal repolarisation

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44
Q

what are the 4 situations you can see t wave inversion in?

A

ischaemia

ventricular hypertrophy

bundle branch block

digoxin treatment

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45
Q

what does low sodium do to the ecg

A

it doesn’t change the ecg at all

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46
Q

low k+ causes what ecg changes

A

T wave flattening

hump on the end of the T wave called the U wave

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47
Q

high potassium does what to the ecg

A

peaked t waves with disappearance of the ST segment

QRS may be widened

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48
Q

low calcium does what to the ecg

A

long qt

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49
Q

high calcium does what to the ecg

A

short qt

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50
Q

what investigations for angina

A

ECG

FBC

lipid profile

HbA1c

LFTs (before statins)

U&E (before ACEIs)

TFTs

CT Coronary angiography

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51
Q

management of angina

A
  • 1st line:
    • lifestyle advice
  • secondary prevention:
    • antiplatelet
      • aspirin OR clopidogrel
      • OR aspirin AND clopidogrel
    • statin
      • atorvastatin 10mg PO OD
  • if symptomatic:
    • sublingual GTN spray +/-
    • beta blocker (metoprolol) +/-
    • calcium channel blocker (nifedipine) +/-
    • long acting nitrate (isosorbide mononitrate PO)
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52
Q

explain PCI

A

Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent) is offered to patients with “proximal or extensive disease” on CT coronary angiography. This involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.

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53
Q

explain cabg

A

Coronary Artery Bypass Graft (CABG) surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI.

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54
Q

the right coronary artery supplies the

A
  • Right atrium
  • Right ventricle
  • Inferior aspect of left ventricle
  • Posterior septal area
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55
Q

the circumflex artery supplies the

A
  • Left atrium
  • Posterior aspect of left ventricle
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56
Q

the left anterior descending artery supplies the

A
  • Anterior aspect of left ventricle
  • Anterior aspect of septum
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57
Q

different sub-devisions of acs

A
  • if there’s st elevation or new LBBB it’s a stemi
  • it’s nstemi if no st elivation but trops are high OR there’s other ecg changes such as
    • st depression
    • t wave inversion
    • pathological q waves
  • if trops normal and there’s no pathological changes on ecg then it’s unstable angina or another cause such as MSK
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58
Q

anterolateral infarct is likely which artery and would show in which leads

A

left coronary artery

aVL, V3-6, I

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59
Q

anterior infarct is likely which artery and would show in which leads

A

LAD

V1-4

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60
Q

lateral infarct is likely which artery and would show in which leads

A

I, aVL, V5-6

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61
Q

inferior infarct is likely which artery and would show in which leads?

A

right coronary artery

II, III and aVF

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62
Q

alternative causes of raised troponins

A
  • Chronic renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
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63
Q

what are serial troponins

A

baseline and 6 or 12 hours after onset of symptoms

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64
Q

explain thrombolysis

A

Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

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65
Q

ideal treatment for STEMI

A

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:

  • Primary PCI (if available within 2 hours of presentation)
  • Thrombolysis (if PCI not available within 2 hours)

The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor).

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66
Q

acute nstemi treatment

A
  • BATMAN

B – Beta-blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

M – Morphine titrated to control pain

A – Anticoagulant: Fondaparinux (unless high bleeding risk)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

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67
Q

scoring system for NSTEMI mortality and what it means for treatment

A

GRACE Score

  • <5% Low Risk
  • 5-10% Medium Risk
  • >10% High Risk

If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

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68
Q

what’s included in the grace score

A

Age

Heart rate/pulse

Systolic BP

Creatinine

Cardiac arrest at admission

CHF

Pulmonary edema

Cardiogenic shock

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69
Q

what is dressler’s syndrome?

A
  • occurs about 2-3 weeks after an MI
  • it’s an autoimmune pericarditis
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70
Q

how does dressler’s syndrome present?

A

pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade

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71
Q

how do you diagnose dressler’s syndrome?

A

diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

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72
Q

management of dressler’s syndrome

A

NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.

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73
Q

triggers for acute left ventricular failure

A
  • Iatrogenic (e.g. too much fluids in an elderly patient with poor LV function)
  • Sepsis
  • MI
  • Arrhythmias
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74
Q

what is the function of BNP

A

To relax the smooth muscle in blood vessels. This reduces the systemic vascular resistance making it easier for the heart to pump blood through the system.

BNP also acts on the kidneys as a diuretic to promote the excretion of more water in the urine. This reduces the circulating volume helping to improve the function of the heart.

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75
Q

non heart failure causes of a raised BNP

A
  • Tachycardia
  • Sepsis
  • Pulmonary embolism
  • Renal impairment
  • COPD

it is very sensitive not specific

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76
Q

work up for acute LVF

A
  • ECG (to look for ischaemia and arrhythmias)
  • Arterial Blood Gas (ABG)
  • Chest Xray
  • Bloods (routine bloods for infection, kidney function, BNP and consider troponin if suspecting MI)
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77
Q

presentation of acute left ventricular failure

A
  • Shortness of breath
  • Cough (frothy white/pink sputum)
  • Reduced oxygen saturations
  • 3rd Heart Sound
  • Bilateral basal crackles (sounding “wet”) on auscultation
  • Hypotension in severe cases (cardiogenic shock)

There may also be signs and symptoms related to underlying cause, for example:

  • Chest pain in ACS
  • Fever in sepsis
  • Palpitations in arrhythmias
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78
Q

what is a normal ejection fraction

A

anything above 50%

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79
Q

normal pulmonary artery pressure at rest

A

18 to 25 mmHg

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80
Q

heart failure chest x ray findings

A
  • dilated upper airway vessels (upper lobe diversion)
  • cardiomegaly (cardiothoracic ratio of >0.5)
  • kerly B lines
  • bilateral pleural effusions
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81
Q

management of acute left ventricular failure

A
  • Pour SOD
    • Pour away (stop) IV fluids
    • Sit the patient upright
    • Oxygen
    • Diuretics (e.g. 40mg IV furosemide)
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82
Q

why does PND happen at night

A
  • fluid over larger area as laid down
  • respiratory centre is less responsive during sleep: resp effort doesn’t increase in response to hypoxia
  • less adrenaline during sleep so myocardium is more relaxed and cardiac output is worse
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83
Q

what are the different types of heart failure

A
  • heart failure with reduced ejection fraction
    • LVEF <40%
  • heart failure with mid range ejection fraction
    • LVEF 40%-49%
    • raised BNP
    • and at least one other criterion
      • relevant structural heart disease (e.g., left ventricular hypertrophy [LVH] or left atrial enlargement),
      • diastolic dysfunction
  • heart failure with preserved ejection fraction
    • LVEF >50%
    • raised BNP
    • and at least one other criterion
      • relevant structural heart disease
      • diastolic dysfunction
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84
Q

NHYA heart failure classification

A

Class I: Mild. No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, or dyspnoea.

Class II: Mild. Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitations, or dyspnoea.

Class III: Moderate. Marked limitation of physical activity. Comfortable at rest, but gentle activity causes fatigue, palpitations, or dyspnoea.

Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

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85
Q

when to refer chronic heart failure

A
  • refer those with NT-proBNP above 2000 to a specialist for an echo within two weeks
  • if between 400-2000 then they need an echo within 6 weeks
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86
Q

management of acute heart failure with reduced ejection fraction

A
  • Furosemide titrated according to symptoms
  • prescribe both an ace inhibitor and a B blocker but one at a time
    • if fluid overload an ace inhibitor first
      • if cant tolerate then an ARB
    • if angina then a B blocker first
  • aldosterone antagonist if not controlled with above
    • spironolactone or eplerenone
  • also
    • yearly flu and pneumococcal vaccine
    • exercise rehab group for heart failure
    • treat cause if known e.g. surgical treatment of valve problems
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87
Q

what is cor pulmonale

A

right sided heart failure caused by respiratory disease

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88
Q

what are the cause of cor pulmonale

A
  • COPD is the most common cause
  • Pulmonary Embolism
  • Interstitial Lung Disease
  • Cystic Fibrosis
  • Primary Pulmonary Hypertension
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89
Q

why might you get pulsatile hepatomegaly

A

in right sided heart failure with tricuspid regurgitation

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90
Q

above what threshold do you diagnose hypertension

A

blood pressure above 140/90 in clinic or 135/85 with ambulatory or home readings.

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91
Q

what is the difference between primary (essential) and secondary hypertension? what is more common?

A

primary (essential hypertension) is 95% of all hypertension and means there is not a known cause

secondary hypertension has a known cause

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92
Q

causes of secondary hypertension

A
  • Consider in patients aged under 40
  • Remember with the mnemonic ROPE
    • R – Renal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider renal artery stenosis.
    • O – Obesity
    • P – Pregnancy induced hypertension / pre-eclampsia
    • E – Endocrine. Most endocrine conditions can cause hypertension
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93
Q

main endocrine consideration for secondary hypertension

A

hyperaldosteronism (“Conns syndrome”) as this may represent 2.5% of new hypertension. A simple test for this is a renin:aldosterone ratio blood test.

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94
Q

patients with type two diabetes should have hypertension screenings how frequently?

A

every year

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95
Q

how frequently should the general population be screened for high blood pressure?

A

every five years

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96
Q

what investigations should all patients with new diagnoses of hypertension get

A
  • Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
  • Bloods for HbA1c, renal function and lipids
  • Fundus examination for hypertensive retinopathy
  • ECG for cardiac abnormalities
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97
Q

what are the different stages of hypertension

A
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98
Q

do the flow diagram for hypertension treatment

A
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99
Q

blood pressure targets in people under 80

A

Clinic BP: <140/90 mmHg

ABPM/HBPM: <135/85 mmHg

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100
Q

blood pressure targets in people over 80

A

Clinic BP: <150/90 mmHg

ABPM/HBPM: <145/85 mmHg

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101
Q

what is the third heart sound

A

it’s the chordae tendonae twanging open like guitar string

can be normal in people aged 15-40

can indicate heart failure in people over 40

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102
Q

what are the 4 valve areas on the chest

A
  • Pulmonary: 2nd I.C.S left sternal border
  • Aortic: 2nd I.C.S right sternal border
  • Tricuspid: 5th I.C.S left sternal border
  • Mitral: 5th I.C.S mid clavicular line (apex area)
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103
Q

what are the special manoeuvres for listening to certain murmurs

A
  • Patient on their left hand side (mitral stenosis)
  • Patient sat up, learning forward and holding exhalation (aortic regurgitation)
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104
Q

mitral stenosis is caused by

A
  • Rheumatic Heart Disease
  • Infective Endocarditis
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105
Q

what kind of murmur is mitral stenosis

A

mid-diastolic, low pitched “rumbling” murmur due to a low velocity of blood flow. There will be a loud S1 due to thick valves requiring a large systolic force to shut, then shutting suddenly

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106
Q

describe the sound of mitral regurgitation

A

pan-systolic, high pitched “whistling” murmur due to high velocity blood flow through the leaky valve. The murmur radiates to left axilla. You may hear a third heart sound.

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107
Q

causes of mitral regurgitation

A
  • Idiopathic weakening of the valve with age
  • Ischaemic heart disease
  • Infective Endocarditis
  • Rheumatic Heart Disease
  • Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
108
Q

describe the murmur in aortic stenosis

A

ejection-systolic, high pitched murmur (high velocity of systole). This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole

radiates into the carotids

109
Q

causes of aortic stenosis

A
  • Idiopathic age related calcification
  • Rheumatic Heart Disease
110
Q

what is an austin flint murmur

A

heard at the apex and is an early diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate.

111
Q

what are the causes of aortic regurgitation

A
  • Idiopathic age related weakness
  • Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
112
Q

where do bioprosthetic heart valves come from and how long do they last

A

they come from pigs and they last around 10 years

113
Q

how long do mechanical heart valves last

A

well over 20 years

114
Q

what is the target INR if someone has a mechanical heart valve

A

2.5-3.5

115
Q

major complications of mechanical heart valves

A
  • Thrombus formation (blood stagnates and clots)
  • Infective endocarditis (infection in prosthesis)
  • Haemolysis causing anaemia (blood gets churned up in the valve)
116
Q

A click replaces S1 for metallic valve replacing which valve

A

mitral

117
Q

A click replaces S1 for metallic valve replacing which valve

A

aortic

118
Q

what is tavi the treatment for

A

severe aortic stenosis

119
Q

explain tavi

A

It involves local or general anaesthetic, inserting a catheter in to the femoral artery, feeding a wire under xray guidance to the location of their aortic valve, then inflating a balloon to stretch the stenosed aortic valve and implanting a bioprosthetic valve in the location of the aortic valve.

valve is bioprosthetic so they don’t require warfarin

120
Q

what are the rates of infective endocarditis in valve replacement patients

what are the usual causative organisms

A
  • 2.5% of patients having a surgical valve replacement.
  • 1.5% of patients having TAVI
  • This is usually caused by one of three gram positive cocci organisms:
    • Staphylococcus
    • Streptococcus
    • Enterococcus
121
Q

there are two differentials for an irregularly irregular pulse - what are they?

A
  • Atrial fibrillation
  • Ventricular ectopics
122
Q

what is valvular AF

A

Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the atrial fibrillation. AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as non-valvular AF.

123
Q

what are the most common causes of AF

A
  • remember that AF affects mrs SMITH
  • Sepsis
  • Mitral valve stenosis
  • Ischaemic heart disease
  • Thyrotoxicosis
  • Hypertension
124
Q

draw flow diagram of how to treat AF in the acute setting

A
125
Q

what is the first line treatment for AF

A

rate control with either a beta blocker or a rate limiting calcium channel blocker such as verapamil or diltiazem

126
Q

what do you need to do for all patients with AF

A

CHA2DS2VASc and ORBIT to assess risk of clot/bleeding

127
Q

what is CHA2DS2VASc and how should it be used

A
  • Congestive heart failure = 1
  • Hypertension = 1
  • Age older than or equal to 75 years = 2
  • Diabetes mellitus = 1
  • Stroke/TIA = 2
  • Vascular disease (prior myocardial infarction, peripheral arterial disease, or aortic plaque) = 1
  • Age 65–74 years = 1
  • Sex category (female) = 1

offer anticoagulation with a DOAC if >2 in women or >1 in men

128
Q

what anticoagulation should you use in AF

A

a doac such as rivaroxiban or warfarin if doacs are contraindicated

129
Q

what tool should you use to assess risk of bleeding in a patient with atrial fibrillation

A

ORBIT (it used to be hasbled)

130
Q

what is the orbit risk assessment tool

A
131
Q

in delayed cardioversion how long should they be anticoagulated for and why

A

In delayed cardioversion the patient should be anticoagulated (see below) for a minimum of 3 weeks prior to cardioversion. Anticoagulation is essential because during the 48 hours prior to cardioversion they may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a stroke.

They should have rate control whilst waiting for cardioversion.

132
Q

how do you treat paroxysmal atrial fibrillation

A

patients still need to be anticoagulated according to CHADSVASc

they can also use a pill in the pocket approach for when symptoms come on

the pill of choice is normally flecanide

133
Q

when should you avoid flecanide?

A

Avoid flecanide in atrial flutter as it can cause 1:1 AV conduction and resulting in a significant tachycardia.

134
Q

what is the half life of warfarin

A

1-3 days

135
Q

what is the half life of doacs

A

7-15 hours

136
Q

what can be used to reverse apixaban and rivaroxaban in the case of life threatening bleeding?

A

Andexanet alfa

137
Q

what can be used to reverse dabigatran in the case of life threatening bleeding

A

Idarucizumab

138
Q

which drug should not be used in VT

A

verapamil as it may precipitate cardiac arrest

139
Q

broad complex tachycardias are from where in origin

A
  • they could be supraventricular with aberrant conduction
  • they could also be ventricular in origin
  • in a peri-arrest situation you should assume them to be ventricular in origin
140
Q

what is the definition of ventricular tachycardia

A
  • broad complex tachycardia originating from a ventricular focus
    • 3 or more ventricular extrasystoles in succession at a rate of more than 120 bpm
141
Q

how to treat tachycardia with pulse - draw algorithm

A
142
Q

what’s included in hasbled

A
143
Q

what’s included in hasbled

A
144
Q

what are the four cardiac arrest rhythms and which are shockable

A

Shockable rhythms:

  • Ventricular tachycardia
  • Ventricular fibrillation

Non-shockable rhythms:

  • Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
  • Asystole (no significant electrical activity)
145
Q

Narrow complex tachycardia in a stable patient can be:

how would you treat each?

A
  • Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)
  • Atrial flutter – control rate with a beta blocker
  • Supraventricular tachycardias – treat with vagal manoeuvres and adenosine
146
Q

broad complex tachycardia in a stable patient could be what? and how would you treat each?

A
  • Ventricular tachycardia or unclear – amiodarone infusion
  • If known SVT with bundle branch block treat as normal SVT
  • If irregular may be AF variation – seek expert help
147
Q

what are the rates involved in atrial flutter and why

A
  • atrial flutter is due to a re-entry loop
  • this stimulates atria at 300bpm
  • every second atrial stimulation is conducted to the ventricles
  • this gives a ventricular rate of 150bpm
148
Q

what is the treatment for atrial flutter

A
  • Rate/rhythm control with beta blockers or cardioversion
  • Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
  • Radiofrequency ablation of the re-entrant rhythm
  • Anticoagulation based on CHA2DS2VASc score
149
Q

what are the three types of SVT

A
  • “Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
  • “Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
  • “Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node.
150
Q

how does adenosine work

A
  • Adenosine interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm.
  • It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway.
  • It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return.
151
Q

in which patients should adenosine be avoided

A
  • patients with
    • asthma
    • COPD
    • heart failure
    • heart block
    • severe hypotension
152
Q

how should you administer adenosine

A
  • Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
  • Initially 6mg, then 12mg and further 12mg if no improvement between doses
  • warn about feeling of impending doom
153
Q

what is the definitive treatment for wolff parkinson white syndrome

A

radiofrequency ablation of the bundle of kent

154
Q

how does radiofrequency ablation work

A
  • Catheter ablation is performed in a electrophysiology laboratory, often called a “cath lab”.
  • General anaesthetic
  • Inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart.
  • Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways.
  • The operator may try to induce the arrhythmia to make the abnormal pathways easier to find.
  • Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity.
  • This leaves scar tissue that does not conduct the electrical activity.
155
Q

radiofrequency ablation is curative for which types of arrhythmia

A
  • Atrial Fibrillation
  • Atrial Flutter
  • Supraventricular Tachycardias
  • Wolff-Parkinson-White Syndrome
156
Q

causes of a long QT

A
  • Long QT Syndrome (inherited)
  • Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
  • Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
157
Q

acute management of torsades de pointes

A
  • Correct the cause (electrolyte disturbances or medications)
  • Magnesium infusion (even if they have a normal serum magnesium)
  • Defibrillation if VT occurs
158
Q

what is bigeminy

A
  • it is when a ventricular ectopic happens after every sinus beat
  • so normal sinus beat
    • followed by broad QRS without a P wave
159
Q

draw the bradycardia algorithm

A
160
Q

first line management of acute pericarditis is

A

NSAID and colchicine

161
Q

features of pericarditis

A
  • chest pain: may be pleuritic. Is often relieved by sitting forwards
  • other symptoms include non-productive cough, dyspnoea and flu-like symptoms
  • pericardial rub
  • tachypnoea
  • tachycardia
162
Q

ecg changes in pericarditis

A
  • the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
  • ‘saddle-shaped’ ST elevation
  • PR depression: most specific ECG marker for pericarditis
163
Q

causes of pericarditis

A
  • most common: coxsacie virus
  • TB
  • uraemia (causes fibrinous pericarditis)
  • trauma
  • post MI (dressler’s syndrome)
164
Q

side effects of adenosine

A
  • flushing
  • nausea
  • sweating
  • bronchospasm
  • chest pain
  • feeling of impending doom
165
Q

adenosine half life

A

8-10 seconds

166
Q

what is the investigation of choice if you suspect PE in a patient with renal failure

A

V/Q scan since it uses radio nucleotides rather than contrast (as used in CTPA which would otherwise be gold standard) so there is no risk of further renal impairment

167
Q

what is the investigation of choice if you suspect PE in a pregnant patient

A

V/Q scan since radiation dose from the injected radio-nucleotides is lower than the dose absorbed from CT imaging (so no CTPA)

168
Q

How do you rule out PE

A
  • all perc criteria must be absent
  • you should only use perc when you have a low clinical suspicion of PE
  • HADCLOTS
    • Hormones
    • age >50
    • DVT/PE history
    • Coughing blood
    • Leg swelling
    • O2 <94
    • Tachycardia >100
    • Surgery/trauma in last 4 wks
169
Q

if you suspect PE what score should you do and how do you interpret the results?

A
170
Q

based on someone’s level 2 wells score how should you act

A
  • PE Likely (>4 points)
    • immediate CTPA
    • if CTPA delay then interim therapeutic anticoagulation
      • this means a DOAC since these can be continued if the result is positive
  • if PE unlikely (4 points or less)
    • D-Dimer with result within 4 hours (or ITAC if delay)
      • if D-dimer positive then immediate CTPA
        • if delay in CTPA then give interim therapeutic anticoagulation until scan is performed
      • if D-dimer negative then PE unlikely consider another diagnosis
171
Q

ECG changes in PE

A
  • the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’.
    • However, this change is seen in no more than 20% of patients
  • right bundle branch block and right axis deviation are also associated with PE
  • sinus tachycardia may also be seen
172
Q

Chest x ray findings in PE

A
  • a chest x-ray is recommended for all patients to exclude other pathology
  • however, it is typically normal in PE
  • possible findings include a wedge-shaped opacification
173
Q

Chest x ray findings in PE

A
  • a chest x-ray is recommended for all patients to exclude other pathology
  • however, it is typically normal in PE
  • possible findings include a wedge-shaped opacification
174
Q

What are the first line antihypertensives in diabetics regardless of age

A
  • ACE inhibitors or angiotensin II receptor agonists since they have a renoprotective effect in diabetes
175
Q

features of hypercalcaemia

A
  • ‘bones, stones, groans and psychic moans’
  • corneal calcification
  • shortened QT interval on ECG
  • hypertension
176
Q

What is the most common cause of high calcium

A

cancer

177
Q

what is ABCD2 and what is it used to test

A

Prognostic score for risk stratifying patients who’ve had a suspected TIA

178
Q

how is heart failure classed

A

nyha classification

179
Q

what is DAS28

A

Measure of disease activity in rheumatoid arthritis

  1. count the number of swollen joints (out of the 28),
  2. count the number of tender joints (out of the 28),
  3. take blood to measure the erythrocyte sedimentation rate (ESR) or C reactive protein (CRP),
  4. ask you (the patient) to make a ‘global assessment of health’ (indicated by marking a 10 cm line between very good and very bad).

These results are then fed into a complex mathematical formula to produce the overall disease activity score. A DAS28 of greater than 5.1 implies active disease, less than 3.2 low disease activity, and less than 2.6 remission.

180
Q

what is wells score

A

Helps estimate the risk of a patient having a deep vein thrombosis

181
Q

what are the H’s and the Ts of reversible cardiac arrest

A
182
Q

in ALS you need to give chest compressions and assess for a shockable rhythm every 2 minutes (and administer a shock if it’s shockable) what other treatment should you do

A
  • Give oxygen
  • Intravenous or intraosseous access
  • Give adrenaline every 3–5 min
  • Give amiodarone after 3 shocks
  • Identify and treat reversible causes
183
Q

when do you give adrenaline in ALS and how much by which route

A
  • adrenaline 1 mg as soon as possible for non-shockable rhythms
  • during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
  • repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
  • IV is first line but if not then IO
184
Q

when is amiodarone given in ALS and how much

A
  • amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
  • a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
185
Q

investigations for palpitations

A
  • first line
    • ECG
      • only captures for a few seconds so may miss episodic arrhythmias but may catch linked abnormalities
    • TFTs
    • U&E
    • FBC
  • if nothing found
    • Holter monitoring
  • if nothing found
    • external loop recorder
    • implantable loop recorder
186
Q

what is the inheritance pattern of hypertrophic obstructive cardiomyopathy

A

autosomal dominant

187
Q

what is the most common cause of sudden cardiac death in the young

A

hypertrophic obstructive cardiomyopathy HOCM

188
Q

what is the pathophysiology of hypertrophic obstructive cardiomyopathy

A
  • mutation in gene encoding beta myosin
  • results in diastolic dysfunction
    • left ventricle hypertrophy leads to decreased compliance leads to decreased cardiac output
  • characterised by myofibrillar hypertrophy with chaotic and disorganised fashion myocytes and fibrosis on biopsy
189
Q

features of hypertrophic obstructive cardiomyopathy

A
  • can be asymptomatic
  • angina syncope
    • typically following exercise
      • due to subaortic hypertrophy of ventricular septum resulting in functional aortic stenosis
  • sudden death
  • arrhythmias
  • heart failure
  • ejection systolic murmur
  • jerky pulse with a double apex beat
190
Q

what are the echo findings of hypertrophic obstructive cardiomyopathy

A
  • mnemonic: MR SAM ASH
    • mitral regurge (MR)
    • systolic anterior motion (SAM) of the anterior mitral valve leaflet
    • asymetric hypertrophy (ASH)
191
Q

what are the stages of hypertension

A
192
Q

how do you decide whether to treat hypertension

A
193
Q

how do you manage hypertension

A
194
Q

what are ecg changes and the coronary artery implicated for the following infarctions:

anteroseptal

inferior

anterolateral

lateral

posterior

A
195
Q

what is the first line treatment for heart failure

A

The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker

  • generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first
  • beta-blockers licensed to treat heart failure in the UK include bisoprolol, carvedilol, and nebivolol.
  • ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction
196
Q

what is second line treatment for heart failure

A

Second-line treatment is an aldosterone antagonist

  • Examples include spironolactone and eplerenone
  • it should be remembered that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored
197
Q

what are the third line treatments for heart failure

A
  • Third-line treatment should be initiated by a specialist.
    • digoxin if coexistant AF
    • hydralazine if afrocarribean
    • cardiac resynchronization therapy if broad QRS
198
Q

what are the different criteria for the different third line treatments in heart failure

A
  • ivabradine
    • criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
  • sacubitril-valsartan
    • criteria: left ventricular fraction < 35%
    • is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
    • should be initiated following ACEi or ARB wash-out period
  • digoxin
    • digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
    • it is strongly indicated if there is coexistent atrial fibrillation
  • hydralazine in combination with nitrate
    • this may be particularly indicated in Afro-Caribbean patients
  • cardiac resynchronisation therapy
    • indications include a widened QRS (e.g. left bundle branch block) complex on ECG
199
Q

what are the vaccine requirements for people with heart failure

A
  • offer annual influenza vaccine
  • offer one-off pneumococcal vaccine
    • adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years
200
Q

when might you hear splitting of the first heart sound?

A

when the mitral valve closes significantly before the tricuspid valve, producing two separate audible sounds. Inspiration is a common cause of this as it delays the closure of the tricuspid valve

201
Q

when might you hear a soft second heart sound

A

normally found in patients with aortic stenosis

202
Q

what distinctive heart sound does pulmonary hypertension cause

A

a loud second heart sound as the pulmonary valve shuts hard

203
Q

what is the treatment for torsades de pointes

A

IV magnesium

204
Q

drug management of angina

A
  • all patients should get aspirin and a statin unless contraindicated
  • sublingual GTN PRN
  • then a beta blocker OR calcium channel blocker
    • if ccb monotherapy then rate limiter such as diltiazem or verapamil
  • then b blocker and ccb dual therapy
    • if using b blocker and ccb in combination then use nifedepine (remember that verapamil can’t be used with beta blockers)
  • then consider addition of long acting nitrite such as isosorbide mononitrate while they await assessment for PCI or CABG
205
Q

what is the most common artery affected by peripheral arterial disease

A

femoral artery

206
Q

how do you confirm a diagnosis of peripheral arterial disease

A

doppler ultrasonography

207
Q

what are the different ABPI readings for different levels of limb ischaemia

A

1 = normal

  1. 6-0.9 = claudication
  2. 3-0.6 = rest pain

<0.3 = impending gangrene

208
Q

what are the principle risk factors for peripheral arterial disease

A

smoking and diabetes

209
Q

management of intermittent claudication

A
  • exercise (supervised programme if available)
  • refer for consideration of angioplasty or bypass surgery
  • antiplatelet therapy with aspirin or clopidogrel
210
Q

what are the interventions for acute lower limb ischaemia

A
  • endovascular therapies
    • percutaneous catheter directed thrombolytic therapy
    • percutaneous mechanical thrombus extraction
  • surgical interventions
    • endarterectomy
    • bypass surgery
    • surgical thromboembolectomy
    • amputation if limb is unsalvageable
211
Q

what is acute limb ischaemia

A

a sudden decrease in limb perfusion that threatens limb viability. In acute limb ischaemia, decreased perfusion and symptoms and signs develop over less than 2 weeks.

212
Q

what most commonly causes acute limb ischaemia

A

a thrombosis within a diseased artery when a plaque ruptures

213
Q

what is the definition of an abdominal aneurysm

A

an aortic diameter of 3 cm or greater

214
Q

when would an unruptured AAA be repaired?

A
  • if it is symptomatic
  • if it is asymptomatic but larger than 4.0cm and has grown by more than 1cm in the last year
  • if it is asymptomatic and 5.5cm or larger
215
Q

what is the monitoring for AAA

A
  • 3.0-4.4 cm: annual ultrasound.
  • 4.5-5.4 cm: three-monthly ultrasound.
  • 5.5 cm or bigger - consider surgery (see below): or three-monthly ultrasound.
216
Q

how are AAAs repaired

A
  • open surgical repair
    • aortic and iliac clamping
    • removal or aneurysmal segment
    • replacement with a prosthetic graft
  • endovascular repair of AAA (EVAR)
    • stent graft system introduced through femoral arteries
217
Q

what is AAA screening

A

screening by ultrasound for men aged 65 - if negative this rules out AAA for life

218
Q

is AAA more common in men or women

A

it is 6 times more common in men

219
Q

what are the specific causes of AAA

A
  • Trauma.
  • Infection - brucellosis, salmonellosis, tuberculosis, HIV.
  • Inflammatory diseases - eg, Behçet’s disease, Takayasu’s disease. Inflammatory aneurysms may have multifactorial pathology[5].
  • Connective tissue disorders - Marfan’s syndrome, Ehlers-Danlos syndrome type IV.
220
Q

what are the causes of TAA

A
  • Genetic
    • In some families, there appears to be an autosomal dominant trait causing TAA
  • Certain connective tissue disorders:
    • Marfan’s syndrome.
    • Ehlers-Danlos syndrome type IV
  • Infections:
    • Tertiary syphilis
    • Mycotic aneurysm[8]
    • HIV[9]
  • Aortitis
  • giant cell arteritis
  • rheumatoid arthritis
  • Behçet’s disease
  • Takayasu’s arteritis
  • Trauma.
  • Weightlifting, cocaine and amfetamine use
    • perhaps because of the large rises in blood pressure which occur during these activities.
221
Q

best imaging for AAA and TAA

A

CT scan with contrast as detailed views are needed for repair planning

222
Q

who needs surgery for an unruptured TAA

A
  • If it’s symptomatic regardless of size then it needs surgery
  • asumptomatic TAAs with diameter >5.5 ascending aorta and >6cm descending aorta
  • patients with strong family history or marfans may need surgery sooner
223
Q

what is the most common risk factor for aortic dissection

A

hypertension

224
Q

what are the important features about the pain in aortic dissection

A
  • pain is abrupt and maximal at onset unlike in MI
  • pain migrates as dissection progresses
  • proximal dissections - pain retrosternal
  • distal dissections - pain between scapulae
  • described as sharp, tearing and ripping
225
Q

what is the secondary prevention of ACS

A
  • patients who have had ACS require lifelong treatment to reduce risk of another event - this includes:
    • aspirin
    • clopidogrel
    • beta blocker
    • ace inhibitor
    • staitin
226
Q

what is the secondary prevention of ACS

A
  • patients who have had ACS require lifelong treatment to reduce risk of another event - this includes:
    • aspirin
    • clopidogrel
    • beta blocker
    • ace inhibitor
    • staitin
227
Q

what are the stemi criteria

A
  • clinical symptoms consistent with ACS ECG features in ≥ 2 contiguous leads of:
    • ≥ 2.5 small squares ST elevation in leads V2-3 in men under 40 years, or ≥ 2 small squares ST elevation in leads V2-3 in men over 40 years
    • 1.5 small square ST elevation in V2-3 in women
    • 1 small square ST elevation in other leads
    • new LBBB (LBBB should be considered new unless there is evidence otherwise)
228
Q

what is stemi management

A
  • notes
    • it means if PCI is going to take longer than 120 minutes to organise then give fibrinolysis instead
      • an ecg should be done 60-90 minutes after fibrinolysis and if they still have ST elevation then consider PCI
229
Q

what is NSTEMI and ACS management

A
230
Q

how do you assess risk of future cardiac events in patients with ACS

A
  • GRACE score which uses the following factors
    • age
    • heart rate, blood pressure
    • cardiac (Killip class) and renal function (serum creatinine)
    • cardiac arrest on presentation
    • ECG findings
    • troponin levels
231
Q

where is venous ulceration seen typically

A

above the medial malleolus

232
Q

management of venous ulcers

A
  • compression bandaging, usually four layer (only treatment shown to be of real benefit)
  • oral pentoxifylline, a peripheral vasodilator, improves healing rate
233
Q

what are the features of arterial ulcers

A
  • Occur on the toes and heel
  • Painful
  • There may be areas of gangrene
  • Cold with no palpable pulses
  • Low ABPI measurements
234
Q

are venous ulcers typically painful?

A

no typically painful

235
Q

what is the inheritance pattern of haemochromatosis

A

AR

236
Q

what gene is implicated in haemochromatosis

A

HFE - needs both copies to be mutated

237
Q

presenting features of haemochromatosis

A
  • early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
  • ‘bronze’ skin pigmentation
  • diabetes mellitus
  • liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
  • cardiac failure (2nd to dilated cardiomyopathy)
  • hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
  • arthritis (especially of the hands)
238
Q

which complications of haemochromatosis are reversible and which are non-reversible

A
239
Q

what are the diagnostic tests for haemochromatosis

A
  • liver biopsy - perl’s stain
  • molecular genetic testing
240
Q

what would iron studies in someone with haemochromatosis be

A
  • transferrin saturation > 55% in men or > 50% in women
  • raised ferritin (e.g. > 500 ug/l) and iron
  • low TIBC
241
Q

management of haemochromatosisq

A
  • venesection is first line
  • desferrioxamine as second line
242
Q

what is the most common risk factor for infective endocarditis

A

previous episode of endocarditis

243
Q

infective endocarditis in IVDUs typically affects which valve

A

tricuspid

244
Q

most common causative organisms of infective endocarditis

A
  • staphylococcus aureus - most common
  • strep viridans - most common in developing world
245
Q

culture negative causes of infective endocarditis

A
  • prior antibiotic therapy
  • Coxiella burnetii
  • Bartonella
  • Brucella
246
Q

infective endocarditis can be diagnosed with what combination of the duke criteria

A
  • pathological criteria positive, or
  • 2 major criteria, or
  • 1 major and 3 minor criteria, or
  • 5 minor criteria
247
Q

what are the pathological criteria of the duke criteria

A

Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

248
Q

what are the major criteria for duke criteria

A
  • positive blood cultures
    • two if organism specific for IE (such as strep viridans)
    • three if less specific organism - must be taken 12 hrs apart
  • evidence of endocardial involvement
    • new valvular regurge
    • positive echo
249
Q

what are the minor criteria for duke criteria

A
  • predisposing heart condition or intravenous drug use
  • microbiological evidence does not meet major criteria
  • fever > 38ºC
  • vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  • immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
250
Q

what is the initial blind therapy for infective endocarditis

A
  • if native valve
    • amoxicillin, consider adding low-dose gentamicin
  • If penicillin allergic, MRSA or severe sepsis
    • vancomycin + low-dose gentamicin
  • If prosthetic valve
    • vancomycin + rifampicin + low-dose gentamicin
251
Q

what are the three types of ischaemia to the lower GI tract

A
  • acute mesenteric ischaemia
  • chronic mesenteric ischaemia
  • ischaemic colitis
252
Q

how do you diagnose bowel ischaemia

A

CT

253
Q

What causes acute mesenteric ischaemia

A

embolism resulting in occlusion of an artery which supplies the small bowel - for example the superior mesenteric artery

patients classically have a history of AF

254
Q

what is the management of acute mesenteric ischaemia

A

urgent surgery - poor prognosis if surgery’s delayed

255
Q

what is ischaemic colitis and why does it typically occur where it typically does

A

Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage.

It is more likely to occur in ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.

256
Q

management for ischaemic colitis

A
  • usually supportive
  • surgery may be required in a minority of cases if conservative measures fail. Indications would include:
  • generalised peritonitis,
  • perforation or
  • ongoing haemorrhage
257
Q

causes of myocarditis

A
  • viral: coxsackie B, HIV
  • bacteria: diphtheria, clostridia
  • spirochaetes: Lyme disease
  • protozoa: Chagas’ disease, toxoplasmosis
  • autoimmune
  • drugs: doxorubicin
258
Q

what is the classic presentation of myocarditis

A
  • usually young patient with an acute history
  • chest pain
  • dyspnoea
  • arrhythmias
259
Q

what will the bloods show in myocarditis

A
  • ↑ inflammatory markers in 99%
  • ↑ cardiac enzymes
  • ↑ BNP
260
Q

what is the management of myocarditis

A
  • treatment of underlying cause e.g. antibiotics if bacterial cause
  • supportive treatment e.g. of heart failure or arrhythmias
261
Q

what are the complications of myocarditis

A
  • heart failure
  • arrhythmia, possibly leading to sudden death
  • dilated cardiomyopathy: usually a late complication
262
Q

what are the features of acute pericarditis

A
  • chest pain: may be pleuritic. Is often relieved by sitting forwards
  • other symptoms include non-productive cough, dyspnoea and flu-like symptoms
  • pericardial rub
  • tachypnoea
  • tachycardia
263
Q

what are the causes of pericarditis

A
  • viral infections (Coxsackie)
  • tuberculosis
  • uraemia (causes ‘fibrinous’ pericarditis)
  • trauma
  • post-myocardial infarction, Dressler’s syndrome
  • connective tissue disease
  • hypothyroidism
  • malignancy
264
Q

ECG changes of acute pericarditis

A

widespread saddle shaped st elevation

pr depression - most specific pericarditis marker

265
Q

what is the management of pericarditis

A

treat cause if known

combination of NSAIDS and colchicine is now generally used to treat idiopathic or viral pericarditis

266
Q

which is a cause of pericarditis that is most likely to cause constrictive pericarditis

A

TB

Finals (19 decks)

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